Interleukin-6 (IL-6) is one of the main pro-inflammatory cytokines that injured cells in the spinal cord release. The role of this cytokine in both injury and recovery is not well-understood. Other studies suggest that IL-6 can contribute to injury but also plays a role in stimulating tissue repair. The authors used an antibody against the IL-6 receptor to block the effects of IL-6 in mouse and found that this treatment suppressed secondary injury, inflammation, and glial scar formation.

[*] Nakamura M, Okada S, Toyama Y and Okano H (2005). Role of IL-6 in spinal cord injury in a mouse model. Clin Rev Allergy Immunol 28: 197-204. In recent years, various studies have been conducted toward the goal of achieving regeneration of the central nervous system using neural stem cells. However, various complex factors are involved in the regulation of neural stem cell differentiation, and many unresolved questions remain. It has been reported that after spinal cord injury, the intrinsic neural stem cells do not differentiate into neurons but, rather, into astrocytes, resulting in the formation of glial scars. Based on reports that the expression of interleukin (IL)-6 and the IL-6 receptor (IL- 6R) is sharply increased in the acute stages after spinal cord injury and that IL-6 may serve as a factor strongly inducing the differentiation of neural stem cells into astrocytes, we examined the effects of an antibody to IL-6R in cases of spinal cord injury and found that the antibody suppressed secondary injury (caused by inflammatory reactions) and glial scar formation, facilitating functional recovery. This article presents the data from this investigation and discusses the relationship between IL-6 signals and spinal cord injury. Department of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan; Core Research for Evolutional Science and Technology (CREST), Japan Society and Technology Agency (JST), Saitama, Japan.